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. 2021 Jul 21;12:4442. doi: 10.1038/s41467-021-24743-z

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© The Author(s) 2021, corrected publication 2021

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 6 — Wild-type or Rnf20fx/fx newborn pups were injected with a high dose of AAV9-TnT-Cre. P7 heart apexes were used for H3K4me3 and H3K36me3 ChIP-seq. a, b H3K4me3 and H3K36me3 marked active TSSs and gene bodies in control and knockout hearts. The overall distribution pattern of these marks was not altered by Rnf20 inactivation. c, d H3K4me3 signal at each TSS and H3K36me3 signal at each gene was quantified in wild-type and Rnf20 KO groups (upper panel). GSEA revealed that the set of genes that were downregulated in RNF Cas-KO were strongly enriched for genes with reduced H3K4me3 or H3K36me3 signal in Rnf20 KO (lower panel; P < 0.001; NES = normalized enrichment score calculated by GSEA that corrects for gene set size). e, f IGV genome browser views at Myh6 and Tnni3 (red boxes), which are involved in maturational sarcomere isoform switching. These genes were downregulated in RNF Cas-KO and had reduced H3K4me3 and H3K36me3 occupancy in Rnf20 KO. Source data are provided as a Source Data file.